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논문 기본 정보

자료유형
학술저널
저자정보
Ji-Young Yoon (Department of Dental Anesthesia and Pain Medicine Pusan National University Dental Hospital) Do-Wan Kim (Department of Dental Anesthesia and Pain MedicinePusan University) Ji-Hye Ahn (Department of Dental Anesthesia and Pain Medicine School of Dentistry Pusan National University) Eun-Ji Choi (Department of Anesthesia and Pain Medicine School of Medicine Pusan National University Yangsan) Yeon Ha Kim (Department of Integrated Biological Science Pusan National University Busan Korea) 전문정 (부산대학교) 김은정 (Department of Dental Anesthesia and Pain Medicine Pusan National University Dental Hospital Dental)
저널정보
한국조직공학과 재생의학회 조직공학과 재생의학 조직공학과 재생의학 제16권 제3호
발행연도
2019.1
수록면
301 - 309 (9page)

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BACKGROUND: Preterm labor is a leading risk factor for neonatal death and long-term impairment and linked closely with inflammation. Non-obstetric surgery is occasionally needed during pregnancy and the anesthetic drugs or surgery itself can give rise to inflammation. Here, we examined the influence of propofol pretreatment on the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) after lipopolysaccharide (LPS) stimulation. In addition, we evaluated the expression of pro-inflammatory cytokines and nuclear factor kappa B (NF-jB). METHODS: Human amnion-derived WISH cells were used to investigate the effect of propofol on the LPS-induced expression of inflammatory substances involved in preterm labor. For the experiment, WISH cells were pretreated with various concentrations propofol (0.01–10 lg/ml) for 1 h and then treated with LPS (1 lg/ml) for 24 h. Cytotoxicity was evaluated using MTT assay. PGE2 concentration was assessed by ELISA. Protein expressions of COX-2, PGE2 and NF-jB were analyzed by western blotting analysis. RT-PCR was used for analysis of mRNA expression of COX-2, PGE2, interlukin (IL)-1b and tumor necrosis factor (TNF)-a. RESULTS: Propofol showed no cytotoxicity on the WISH cells. LPS-induced PGE2 production and COX-2 and PGE2 expression were decreased after propofol pretreatment. Propofol also attenuated the LPS-induced mRNA expression of IL- 1b and TNF-a. Moreover, the activation of NF-jB was inhibited by propofol pretreatment on LPS-stimulated WISH cells. CONCLUSION: We demonstrated that propofol suppresses the expression of inflammatory substances enhanced by LPS stimulation. Furthermore, this inhibitory effect of propofol on the inflammatory substance expression is mediated by suppression of NF-jB activation.

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